The development of the central nervous system and its functional output, behavior, reflect a series of maturational events that are highly ordered and precisely timed; the consequences of early disruption can be acute and severe or more subtle and insidious. Neonatal exposure to chlordecone, a prototypic organochlorine, produced tremor and increased reflex reactivity in preweaning rodents, effects similar to those observed in acute toxicity studies with adult animals. Sex-dependent body weight changes persisting into adulthood strongly implicated alteration(s) in the sexual differentiation of hypothalamic centers involved in feeding and weight regulation. Long-term alterations in brain catecholaminergic and serotonergic function were suggested by specific pharmacological challenges. Deficits in retention of learned responses dissociable from nonspecific alterations, such as hyperactivity, were also uncovered. Both short- (hypersecretion) and long-term (depression in basal levels) alterations in circulating and adrenal steroids indicated that chlordecone-induced changes in behavioral reactivity and the modulation of memory were produced, at least in part, by acting on the adrenal gland and the feedback regulation of the hypothalamic-pituitary-adrenal axis. Neonatal exposure to triethyl lead (TEL), a representative organometal, was shown to permanently affect behavioral processes in a manner similar to that observed after damage to the septal-hippocampal system. Long-term behavioral alterations were independent of sensory modality and represented a hyperreactive response of the animal to the test environment. Preferential and permanent destruction of hippocampal pyramidal cell fields (regio inferior) were observed under light microscopy. Pharmacological probes suggested long-term alterations in cholinergic, but not dopaminergic, function.